Iodine Articles 8

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Use of iodo-niacin for retinal or vitreous hemorrhages and vitreous floaters.
            (Abrahamson, 1956)  Download
The use of iodine preparations for the pur­ pose of absorbing intraocular hemorrhages and strengthening damaged vascular walls has been known and used extensively for many years but, for some season, has re­ cently fallen into more or less disrepute. In fact, the treatment of recurrent and massive vitreal and retinal hemorrhages and vitreous floaters has been relatively unsatisfactory with the drugs at our disposal.

Is iodine a gatekeeper of the integrity of the mammary gland
            (Aceves et al., 2005)  Download
This paper reviews evidence showing iodine as an antioxidant and antiproliferative agent contributing to the integrity of normal mammary gland. Seaweed is an important dietary component in Asian communities and a rich source of iodine in several chemical forms. The high consumption of this element (25 times more than in Occident) has been associated with the low incidence of benign and cancer breast disease in Japanese women. In animal and human studies, molecular iodine (I(2)) supplementation exerts a suppressive effect on the development and size of both benign and cancer neoplasias. This effect is accompanied by a significant reduction in cellular lipoperoxidation. Iodine, in addition to its incorporation into thyroid hormones, is bound into antiproliferative iodolipids in the thyroid called iodolactones, which may also play a role in the proliferative control of mammary gland. We propose that an I(2) supplement should be considered as an adjuvant in breast cancer therapy.

The extrathyronine actions of iodine as antioxidant, apoptotic, and differentiation factor in various tissues.
            (Aceves et al., 2013) Download
BACKGROUND:  Seaweed is an important dietary component and a rich source of iodine in several chemical forms in Asian communities. Their high consumption of this element (25 times higher than in Western countries) has been associated with the low incidence of benign and cancerous breast and prostate disease in Japanese people. SUMMARY:  We review evidence showing that, in addition to being a component of the thyroid hormone, iodine can be an antioxidant as well as an antiproliferative and differentiation agent that helps to maintain the integrity of several organs with the ability to take up iodine. In animal and human studies, molecular iodine (I2) supplementation exerts a suppressive effect on the development and size of both benign and cancerous neoplasias. Investigations by several groups have demonstrated that these effects can be mediated by a variety of mechanisms and pathways, including direct actions, in which the oxidized iodine dissipates the mitochondrial membrane potential, thereby triggering mitochondrion-mediated apoptosis, and indirect effects through iodolipid formation and the activation of peroxisome proliferator-activated receptors type gamma, which, in turn, trigger apoptotic or differentiation pathways. CONCLUSIONS:  We propose that the International Council for the Control of Iodine Deficient Disorders recommend that iodine intake be increased to at least 3 mg/day of I2 in specific pathologies to obtain the potential extrathyroidal benefits described in the present review.

Induction of experimental mammary carcinogenesis in rats with 7,12-dimethylbenz(a)anthracene.
            (Barros et al., 2004)  Download
PURPOSE:  To test an experimental model of chemical mammary carcinogenesis induction in rats. METHODS:  Twenty young virgin Sprague-Dawley female rats, aged 47 days, received 20 mg of 7,12-dimethylbenz(a)anthracene (DMBA) intragastrically by gavage. Afterwards, at 8 and 13 weeks, their mammary glands were examined. At the end of the experiment, the animals were sacrificed, and the mammary tumors were measured and weighed. Tumor fragments were analyzed using light microscopy. RESULTS:  Eight weeks after DMBA injection, 16 rats presented at least 1 breast tumor (80%). After 13 weeks, all of them (100%) developed breast carcinomas that were confirmed by histopathological analysis. CONCLUSION:  This experimental animal model of chemical mammary induced carcinogenesis is feasible and can be used in further experiments on the role of tumorigenic biomodulator substances.

Mammary gland dysplasia in iodine deficiency. Studies in rats.
            (Eskin et al., 1967) Download
Epidemiological studies suggest that persons living in areas of normal iodine availability show less breast cancer than those living in iodine-deficient areas.1,2 World Health Organization investigations, recently published,3 have revealed that a large segment of the population in the United States and other parts of the world lives in areas of limited iodine availability. In addition, there appears to be statistical evidence of an increased incidence of breast malignancy in hypothyroidism.4-6 Our results imply that iodine deficiency may be involved in these thyroid-breast relationships. The breasts of chronically iodine-deficient female rats treated with testosterone were observed to be considerably larger than their normally fed, testosterone-injected litter-mate controls. No reports directly pertaining to this observation were found in the literature. Therefore, we decided to carry out a systematic investigation of the influence of iodine deficiency on the resting and sex-hormone-treated breasts of female rats.

 

Induction of breast cancer in altered thyroid states
            (Eskin et al., 1968) Download
The development of mammary tumours in rats by orally feeding the chemical carcinogen 7, 12-dimethylbenz (a)-anthracene (DMBA) has been shown to be influenced by the hormonal state of the animal 1. We previously observed that breast dysplasia could be induced in iodine deficient and propylthiouracil (PTU)-treated rats given oestrogen or testosterone 2. Furthermore, the incidence of breast cancer is higher among women with hypothyroidism and in those residing in regions where goitre is endemic 3. The present study considers the …

Resistance of Hormone-Dependent Mammary Cancer to Estrogen Therapy in Altered Thyroid States
            (Eskin and Dratman, 1969) Download
Progesterone fails to prevent the decreased collagen synthesis, the cause was the resultant estrogen deficiency.

Rat mammary gland atypia produced by iodine blockade with perchlorate.
            (Eskin et al., 1975)  Download
Prior published work from our laboratory concluded that there was a need for appropriate metabolic activity of iodine in breast tissue for normal growth and development. Results from studies in rats that were made iodine deficient showed histological changes in the breasts that were atypical and dysplastic. These tissue findings were further affected by the presence of estrogen and thyroxine. These changes parallel the iodine uptake of the tissues, thus representing a difference in the utilization of iodine by the mammary glands. Using an ion blockade agent, sodium perchlorate, breast tissues lacking iodine were evaluated by both endocrine and histological techniques. A dose-response series was completed that showed that perchlorate therapy for 8 weeks at 400 mg/100 ml produced breast blockade by a reduction in iodine uptake of greater than 52% of the control. At these levels, the histological experimentation showed atypia and some pleomorphism of the cells, particularly in the glands of the lobules. Blockade was less effective in estrogen-treated groups. It is especially notable that both histological changes and uptake reduction were greatest in those breasts that had been rendered euthyroid by thyroxine replacement, thus clearly indicating the necessity of iodine itself for maintenance of normal breast development. By this blockade the responses of iodine inadequacy in the breast were shown to cause abnormal tissue changes relative to the percentage of the block obtained.


Dietary iodine and cancer risk.
            (Eskin, 1976)  Download
Sir, the material cited by Dr. Stadel in his hypothesis concerning iodine deficiency and breast cancr risk seems inadequate. Stadels hypothesis: Endocrinological considerations suggest that a low dietary iodine intake may produce a state of increased effective gonadotrophin stimulation, which in turn may produce a hyperoestrogenic state characterised by relatively high production of oestrone and oestradiol and a relatively low oestriol to oestrone plus oestradiol ratio. This altered endocrine state may increase the risk of breast, endometrial, and ovarian cancer. Increasing dietary iodine intake may reduce the risk of these cancers.

Iodine and mammary cancer.
            (Eskin, 1977)  Download
From laboratory studies presented, iodine appears to be a requisite for the normalcy of breast tissue in higher vertebrates. When lacking, the parenchyma in rodents and humans show atypia, dysplasia, and even neoplasia. Iodine-deficient breast tissues are also more susceptible to carcinogen action and promote lesions earlier and in greater profusion. Metabolically, iodine-deficient breasts show changes in RNA/DNA ratios, estrogen receptor proteins, and cytosol iodine levels. Clinically, radionuclide studies have shown that breast atypia and malignancy have increased radioactive iodine uptakes. Imaging of the breasts in high-risk women has localized breast tumors. The potential use of breast iodine determination to determine estrogen dependence of breast cancer has been considered and the role of iodide therapy discussed. In conclusion, iodine appears to be a compulsory element for the breast tissue growth and development. It presents great potential for its use in research directed toward the prevention, diagnosis, and treatment of breast cancer.

The intracellular metabolism of iodine in carcinogenesis.
            (Eskin et al., 1979) Download
Research from this laboratory and others have concluded that significant glandular atypia, and often neoplasia, occurs in the breast tissues of rodents and humans under conditions of iodine deprivation. These cellular changes caused by iodine deficiency are intensified, by aging, steroid hormones, and pituitary hormones. There has been controversy concerning the effect of iodine deficiency on stimulation and maintenance of cancer of the breast in rodents when the cancer is induced chemically or by transplantation. However, neither within this induced neoplastic framework nor with the dysplastic changes seen by deficiency alone have laboratory studies of thepathway of intracellular iodine been previously possible.The new research data addresses the question of whether organification occurs and whether iodine significantly affects the intracellular structures. An hypothesis will be presented that places the inorganic element, iodine, into association with receptor protein complexes that may be responsible for intracellular sex hormone activity. The relationship of this mechanism to carcinogenesis in breast tissue will be considered.

Iodine and breast cancer A 1982 update.
            (Eskin, 1983)  Download
Research has been directed towards investigating the role of the trace element, iodine, in breast cancer etiology, diagnosis, and therapy. In many controled studies, iodine has been established as a requirement for breast tissue normalcy, since deficiency of the element results in histopathology consistent with dysplasia and atypia in rodents. Clinically severe hyperplasia and fibrocystic disease is seen in the breasts of women who have low iodine levels. These precancerous lesions result in a high-risk state as well as persistent symptomatology in women. Iodine replacement therapy has been shown to be efficacious in reducing these conditions in clinical trials. Basic research is directed towards intracellular pathways and metabolism for breast iodide, emulating those seen in the thyroid gland. Thus, using a rat model, iodine intracellular organification is being correlated with risk factors for breast cancer including early and late pregnancies, onset of puberty, menopause, and aging. From our research there is significant evidence that iodine maintains homeostasis in reproductive, effected tissues and is responsible for breast tissue growth and development.

Different tissue responses for iodine and iodide in rat thyroid and mammary glands.
            (Eskin et al., 1995)  Download
This research describes the effects of short-term elemental iodine (I2) and iodide (I-) replacement on thyroid glands and mammary glands of iodine-deficient (ID) Sprague-Dawley female rats. Iodine deficiency causes atypical tissue and physiologic changes in both glands. Tissue histopathology and the endocrine metabolic parameters, such as serum TT4, tissue and body weights, and vaginal smears, are compared. A moderate reduction in thyroid size from the ID control (IDC) was noted with both I- and I2, whereas serum total thyroxine approached the normal control with both I- and I2, but was lower in IDC. Thyroid gland IDC hyperplasia was reduced modestly with I2, but eliminated with I-. Lobular hyperplasia of the mammary glands decreased with I2 and increased with I- when compared with the IDC; extraductal secretions remained the same as IDC with I2, but increased with I-; and periductal fibrosis was markedly reduced with I2, but remained severe with I-. Thus, orally administered I2 or I- in trace doses with similar iodine availability caused different histopathological and endocrine patterns in thyroid and mammary glands of ID rats. The significance of this is that replacement therapy with various forms of iodine are tissue-specific.


Inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis by molecular iodine (I2) but not by iodide (I-) treatment Evidence that I2 prevents cancer promotion.
            (García-Solís et al., 2005)  Download
We analyzed the effect of molecular iodine (I2), potassium iodide (KI) and a subclinical concentration of thyroxine (T4) on the induction and promotion of mammary cancer induced by N-methyl-N-nitrosourea. Virgin Sprague-Dawley rats received short or continuous treatment. Continuous I2 treated rats exhibited a strong and persistent reduction in mammary cancer incidence (30%) compared to controls (72.7%). Interruption of short or long term treatments resulted in a higher incidence in mammary cancer compared to the control groups. The protective effect of I2 was correlated with the highest expression of the I-/Cl- transporter pendrin and with the lowest levels of lipoperoxidation expression in mammary glands. Triiodothyronine serum levels and Na+/I- symporter, lactoperoxidase, or p53 expression did not show any changes. In conclusion continuous I2 treatment has a potent antineoplastic effect on the progression of mammary cancer and its effect may be related to a decrease in the oxidative cell environment.

Iodine prophylaxis--the protective factor against stomach cancer in iodine deficient areas.
            (Gołkowski et al., 2007)  Download
BACKGROUND:  Poland has one of the highest death rates for stomach cancer in Europe. Moderate iodine deficiency and in consequence high goitre prevalence led to the implementation in 1996 of a very efficient mandatory model of iodine prophylaxis, based on household salt iodisation (30 +/- 10 mg KI/1 kg of salt). AIM OF THE STUDY:  The aim of the study was evaluation of incidence rate of stomach cancer and its possible relation to increased iodine consumption in the years 1992-2004. METHODS:  Iodine supply and effectiveness of iodine prophylaxis were evaluated on the basis of comparative analysis of goitre prevalence and ioduria in schoolchildren. To allow comparison between time periods with varying population age structures, the incidence rates of stomach cancer were standardized for age, using the "world standard population". The direct standardization method has been applied. For each sex, the time-trend of incidence rates was shown in graphs over the years 1991-2004. RESULTS:  Evident increase in iodine consumption in this period of time was proved by rise in percentage of schoolchildren (6-8 years old) with ioduria above 100 microg/l from 11.4% in 1992-1993 to 52.9.1% in 2003. It was correlated with the decrease in goitre prevalence from 18.8% to 3.2% respectively. The 24-h thyroid uptake of (131)I in investigated population fell from 45.5% in 1986 to 26.8% in 1998. In Krakow the standardized incidence ratio of stomach cancer for men decreased from 19.1 per 100,000 to 15.7 per 100,000, and for women from 8.3 per 100,000 to 5.9 per 100,000 in the years 1992-2004. A significant decline of average rate of decrease was observed in men and women (2.3% and 4.0% per year respectively). CONCLUSION:  Observed association between improved iodine supply and decrease of incidence of stomach cancer could indicate the protective role against stomach cancer of iodine prophylaxis in iodine deficient areas--further studies are necessary.

A prospective study of iodine status, thyroid function, and prostate cancer risk: follow-up of the First National Health and Nutrition Examination Survey.
            (Hoption Cann et al., 2007) Download
Few studies have investigated the association between iodine status, thyroid disease, and cancer risk despite evidence that thyroid function impacts many organs, including the prostate. We investigated iodine status and prostate cancer risk prospectively using data from the NHANES I Epidemiologic Follow-up Study. Participants were stratified into tertiles according to the urinary iodine/creatinine ratio, as a marker of iodine exposure. As iodine is an integral constituent of thyroid hormones, we also examined the relationship between thyroid disease and prostate cancer risk. Relative to the group with low urinary iodine, the age-adjusted hazard ratio was higher (although marginally insignificant) in the moderate group, hazard ratio 1.33 (95% confidence interval 1.00-1.78), and significantly lower in the high group, 0.71 (0.51-0.99). Thyroid disease was associated with an increased prostate cancer risk, 2.34 (1.24-4.43). Similarly, > 10 yr since thyroid disease diagnosis was associated with an elevated risk, 3.38 (1.66-6.87). After adjusting for other confounding factors, only a history of thyroid disease, 2.16 (1.13-4.14), and > 10 yr since diagnosis of thyroid disease, 3.17 (1.54-6.51) remained significant. Although the role of dietary iodine remains speculative, a role for thyroid disease and/or factors contributing to thyroid disease as a risk factor for prostate carcinogenesis warrants additional investigation.

6-iodolactone, key mediator of antitumoral properties of iodine.
            (Nava-Villalba and Aceves, 2014)   Download
An iodinated derivative of arachidonic acid, 5-hydroxy-6-iodo-8,11,14-eicosatrienoic acid, δ-lactone (6-IL) has been implicated as a possible intermediate in the autoregulation of the thyroid gland by iodine. In addition to antiproliferative and apoptotic effects observed in thyrocytes, this iodolipid could also exert similar actions in cells derived from extrathyroidal tissues like mammary gland, prostate, colon, or the nervous system. In mammary cancer (solid tumors or tumor cell lines), 6-IL has been detected after molecular iodine (I2) supplement, and is a potent activator of peroxisome proliferator-activated receptor type gamma (PPARγ). These observations led us to propose I2 supplement as a novel coadjutant therapy which, by inducing differentiation mechanisms, decreases tumor progression and prevents chemoresistance. Some kinds of tumoral cells, in contrast to normal cells, contain high concentrations of arachidonic acid, making the I2 supplement a potential "magic bullet" that enables local, specific production of 6-IL, which then exerts antineoplastic actions with minimal deleterious effects on normal tissues.

Iodine: deficiency and therapeutic considerations.
            (Patrick, 2008)  Download
Iodine deficiency is generally recognized as the most commonly preventable cause of mental retardation and the most common cause of endocrinopathy (goiter and primary hypothyroidism). Iodine deficiency becomes particularly critical in pregnancy due to the consequences for neurological damage during fetal development as well as during lactation. The safety of therapeutic doses of iodine above the established safe upper limit of 1 mg is evident in the lack of toxicity in the Japanese population that consumes 25 times the median intake of iodine consumption in the United States. Japan's population suffers no demonstrable increased incidence of autoimmune thyroiditis or hypothyroidism. Studies using 3.0- to 6.0-mg doses to effectively treat fibrocystic breast disease may reveal an important role for iodine in maintaining normal breast tissue architecture and function. Iodine may also have important antioxidant functions in breast tissue and other tissues that concentrate iodine via the sodium iodide symporter.

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Antiproliferative/cytotoxic effects of molecular iodine, povidone-iodine and Lugol's solution in different human carcinoma cell lines.
            (Rösner et al., 2016) Download
Clinical trials have revealed that molecular iodine (I2) has beneficial effects in fibrocystic breast disease and in cyclic mastalgia. Likewise, povidone-iodine (PVP-I), which is widely used in clinical practice as an antiseptic agent following tumour surgery, has been demonstrated to have cytotoxic effects on colon cancer and ascites tumour cells. Our previous study indicated that the growth of breast cancer and seven other human malignant cell lines was variably diminished by I2 and iodolactones. With the intention of developing an iodine-based anticancer therapy, the present investigations extended these studies by comparing the cytotoxic capacities of I2, potassium iodide (KJ), PVP-I and Lugol's solution on various human carcinoma cell lines. Upon staining the cell nuclei with Hoechst 33342, the cell densities were determined microscopically. While KJ alone did not affect cell proliferation, it enhanced the antiproliferative activity of I2. In addition, PVP-I significantly inhibited the proliferation of human MCF-7 breast carcinoma, IPC melanoma, and A549 and H1299 lung carcinoma cells in a concentration corresponding to 20 µM I2. Likewise, Lugol's solution in concentrations corresponding to 20-80 µM I2 were observed to reduce the growth of MCF-7 cells. Experiments with fresh human blood samples revealed that the antiproliferative activity of PVP-I and I2 is preserved in blood plasma to a high degree. These findings suggest that PVP-I, Lugol's solution, and a combination of iodide and I2 may be potent agents for use in the development of antitumour strategies.

Iodoprotein formation by rat mammary glands during pregnancy and early postpartum period.
            (Shah et al., 1986) Download
Iodide organification by rat mammary glands was studied during the trimesters of pregnancy and early postpartum period. Organification was followed by measuring trichloroacetic acid (TCA) precipitation of delipidated tissue homogenates. The radiolabeled material was sensitive to proteolytic cleavage by a bacterial protease indicating that the 125I was protein-bound. Gel filtration column chromatography in the presence of sodium dodecyl sulfate (SDS) of delipidated mammary tissue homogenates of pregnant and postpartum rats reproducibly resolved several iodoproteins from free iodide. The Kav value for each iodoprotein peak was calculated and was used to estimate each subunit molecular weight which averaged 37,500, 25,100, and 8500. Another iodoprotein with a very large subunit molecular weight of greater than 300,000 was also detected in mammary tissue. Incorporation of 125I-iodide into the three smaller iodoproteins increased logarithmically from the start of the second trimester of pregnancy through the early postpartum period when approximately 20% of the total 125I uptake by mammary tissue was incorporated into protein. Hyperplasia, acinar development, and intracytoplasmic vacuolization of mammary tissue correlated with the increased incorporation of 125I-iodide into these iodoproteins. The characterization and quantitation of specific iodoproteins in mammary tissue may be important as organification of iodide is believed to be a marker for normal hormone-responsive cells.

A direct relationship between thyroid enlargement and breast cancer.
            (Smyth et al., 1996)  Download
Despite extensive study, evidence to support a direct relationship between diseases of the thyroid and breast has not been established. In this study thyroid volume was assessed by ultrasound in 200 patients with breast cancer and 354 with benign breast disease. Results were compared to appropriate female control groups. Both mean thyroid volume (21.1 +/- 1.4 mL) and the percentage of individual patients with enlarged (> 18.0 mL) thyroid glands (41.5%) were significantly greater in the breast cancer group than equivalent values (13.2 +/- 0.5 mL and 10.5%, respectively) in age-matched controls (P < 0.01 in both cases). The mean thyroid volume of 14.5 +/- 0.34 mL in patients with benign breast disease was also significantly greater than that of 12.5 +/- 0.38 mL in younger controls (P < 0.01). The results support a direct association between breast cancer and increased thyroid volume as mean thyroid volumes and the percentage of individual patients with enlarged thyroid glands were similar in those studied both before (20.8 +/- 1.3 mL and 43.0%) and after (21.4 +/- 1.6 mL and 40.0%) therapies for breast cancer. Although there is no evidence that thyroid enlargement represents a risk factor for breast cancer, the results emphasize the importance of raising the consciousness of the coincidence of both disorders.

Antineoplastic effect of iodine and iodide in dimethylbenz[a]anthracene-induced mammary tumors: association between lactoperoxidase and estrogen-adduct production.
            (Soriano et al., 2011) Download
Several groups, including ours, have reported that iodine exhibited antiproliferative and apoptotic effects in various cancer cells only if this element is supplemented as molecular iodine, or as iodide, to cells that are able to oxidize it with the enzyme thyroperoxidase. In this study, we analyzed the effect of various concentrations of iodine and/or iodide in the dimethylbenz[a]anthracene (DMBA) mammary cancer model in rats. The results show that 0.1% iodine or iodide increases the expression of peroxisome proliferator-activated receptor type γ (PPARγ), triggering caspase-mediated apoptosis pathways in damaged mammary tissue (DMBA-treated mammary gland) as well as in frank mammary tumors, but not in normal mammary gland. DMBA treatment induces the expression of lactoperoxidase, which participates in the antineoplastic effect of iodide and could be involved in the pro-neoplastic effect of estrogens, increasing the formation of DNA adducts. In conclusion, our results show that a supplement of 0.1% molecular iodine/potassium iodide (0.05/0.05%) exert antineoplastic effects, preventing estrogen-induced DNA adducts and inducing apoptosis through PPARγ/caspases in pre-cancer and cancerous cells. Since this iodine concentration does not modify the cytology (histology, apoptosis rate) or physiology (triiodothyronine and thyrotropin) of the thyroid gland, we propose that it be considered as an adjuvant treatment for premenopausal mammary cancer.

More than adequate iodine intake may increase subclinical hypothyroidism and autoimmune thyroiditis: a cross-sectional study based on two Chinese communities with different iodine intake levels.
            (Teng et al., 2011) Download
OBJECTIVE:  With the introduction of iodized salt worldwide, more and more people are exposed to more than adequate iodine intake levels with median urinary iodine excretion (MUI 200-300 μg/l) or excessive iodine intake levels (MUI >300 μg/l). The objective of this study was to explore the associations between more than adequate iodine intake levels and the development of thyroid diseases (e.g. thyroid dysfunction, thyroid autoimmunity, and thyroid structure) in two Chinese populations. DESIGN:  A population-based cross-sectional study was conducted in two areas in which people are exposed to different levels of iodine intake (Rongxing, MUI 261 μg/l; Chengshan, MUI 145 μg/l). A total of 3813 individuals were recruited by random sampling. Thyroid hormones, thyroid autoantibodies in serum, and iodine levels in urine were measured. B-mode ultrasonography of the thyroid was also performed for each participant. RESULTS:  The prevalence of subclinical hypothyroidism was significantly higher for subjects who live in Rongxing than those who live in Chengshan (5.03 vs 1.99%, P<0.001). The prevalence of positive anti-thyroid peroxidase antibody (TPOAb) and positive anti-thyroglobulin antibody (TgAb) was significantly higher for subjects in Rongxing than those in Chengshan (TPOAb: 10.64 vs 8.4%, P=0.02; TgAb: 10.27 vs 7.93%, P=0.01). The increase in thyroid antibodies was most pronounced in the high concentrations of TPOAb (TPOAb: ≥500 IU/ml) and low concentrations of TgAb (TgAb: 40-99 IU/ml) in Rongxing. CONCLUSIONS:  More than adequate iodine intake could be a public health concern in terms of thyroid function and thyroid autoimmunity in the Chinese populations.

Incidence of breast carcinoma in women with thyroid carcinoma.
            (Vassilopoulou-Sellin et al., 1999) Download
BACKGROUND:  Breast carcinoma and differentiated thyroid carcinoma(the most common endocrine malignancy) occur predominantly in women. An association between the two tumors has been suggested by some investigators, but the potential impact of treatment of one of these diseases on the development of the other remains unclear. The authors examined the relation between the occurrence of these two tumors. METHODS:  There were 41,686 patients with breast carcinoma and 3662 with thyroid carcinoma who registered at The University of Texas M. D. Anderson Cancer Center between March 1944 and April 1997. Women who received both diagnoses since 1976 were identified and incidence rates and relative risks of secondary tumor development were calculated. Surveillance, Epidemiology and End Results (SEER) program data on the age-adjusted incidences of these diseases during the same time period were used for the expected incidences in the same population. RESULTS:  Among 18,931 women with a diagnosis of breast carcinoma since 1976, 11 developed differentiated thyroid carcinoma > or = 2 years after the diagnosis of breast carcinoma. These breast carcinoma patients contributed 129,336 person-years of follow-up; the observed incidence of thyroid carcinoma in this group was not different from that in a similar age group of women in the SEER database. Among 1013 women with a diagnosis of thyroid carcinoma since 1976, 24 developed breast carcinoma > or = 2 years after the diagnosis of thyroid carcinoma. These thyroid carcinoma patients contributed 8380 person-years of follow-up; the observed incidence of breast carcinoma in women ages 40-49 years was significantly higher than the expected incidence for women in the same age group in the SEER database. CONCLUSIONS:  Breast carcinoma developing after thyroid carcinoma was diagnosed more frequently than expected in young adult women seen at the study institution since 1976. This potential association and plausible mechanisms of breast carcinoma development after thyroid carcinoma should be evaluated in larger cohorts of patients.


 

A new hypothesis: iodine and gastric cancer.
            (Venturi et al., 1993)  Download
The authors have hypothesized that iodine-deficiency (I-def) or in some cases iodine-excess (I-excess) is associated with the development of gastric cancer. They report a short review of their own work and general literature on this subject in three fields: (1) epidemiology, where geographical and temporal correlations between territories with I-def (or I-excess) endemic goitre and high GC-death rate are reported; (2) immunology, where the possible correlations between I-def, immune-deficiency and GC are reported; and (3) thyroid gland and stomach correlations, both being embryologically derived from primitive gut and able to concentrate iodine. This ability is impaired by nitrates, thiocyanate, salt and by I-excess, which in fact can cause goitre. In our study I-def goitrous people have shown more atrophic gastritis than normal subjects. These data enable us to hypothesize that I-def or I-excess might constitute a new risk factor for gastric cancer, both by regulating gastric trophism and by antagonizing the action of those I-inhibitors (such as nitrates, thiocyanate and salt) previously studied as risk factors for gastric cancer.

Iodide, thyroid and stomach carcinogenesis: evolutionary story of a primitive antioxidant
            (Venturi and Venturi, 1999) Download
The thyroid gland is, embryogenetically and phylogenetically, derived from the primitive gut, and we may consider the thyroid cells as primitive gastroenteric cells which, during evolution, migrated and specialized in the uptake of iodide and in the storage and elaboration of iodine compounds.

 


References

Abrahamson, IA (1956), ‘Use of iodo-niacin for retinal or vitreous hemorrhages and vitreous floaters.’, Am J Ophthalmol, 42 (5), 771-72. PubMed: 13372702
Aceves, C, B Anguiano, and G Delgado (2005), ‘Is iodine a gatekeeper of the integrity of the mammary gland’, J Mammary Gland Biol Neoplasia, 10 (2), 189-96. PubMed: 16025225
——— (2013), ‘The extrathyronine actions of iodine as antioxidant, apoptotic, and differentiation factor in various tissues.’, Thyroid, 23 (8), 938-46. PubMed: 23607319
Barros, AC, et al. (2004), ‘Induction of experimental mammary carcinogenesis in rats with 7,12-dimethylbenz(a)anthracene.’, Rev Hosp Clin Fac Med Sao Paulo, 59 (5), 257-61. PubMed: 15543396
Eskin, BA, et al. (1967), ‘Mammary gland dysplasia in iodine deficiency. Studies in rats.’, JAMA, 200 (8), 691-95. PubMed: 6071498
Eskin, BA, SA Murphey, and MR Dunn (1968), ‘Induction of breast cancer in altered thyroid states’, Nature, 218 1162. PubMed:
Eskin, BA and MB Dratman (1969), ‘Resistance of Hormone-Dependent Mammary Cancer to Estrogen Therapy in Altered Thyroid States’, Proc R Soc Med, 51 218. PubMed:
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——— (1977), ‘Iodine and mammary cancer.’, Adv Exp Med Biol, 91 293-304. PubMed: 343535
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Eskin, BA (1983), ‘Iodine and breast cancer A 1982 update.’, Biol Trace Elem Res, 5 (4-5), 399-412. PubMed: 24263577
Eskin, BA, et al. (1995), ‘Different tissue responses for iodine and iodide in rat thyroid and mammary glands.’, Biol Trace Elem Res, 49 (1), 9-19. PubMed: 7577324
García-Solís, P, et al. (2005), ‘Inhibition of N-methyl-N-nitrosourea-induced mammary carcinogenesis by molecular iodine (I2) but not by iodide (I-) treatment Evidence that I2 prevents cancer promotion.’, Mol Cell Endocrinol, 236 (1-2), 49-57. PubMed: 15922087
Gołkowski, F, et al. (2007), ‘Iodine prophylaxis--the protective factor against stomach cancer in iodine deficient areas.’, Eur J Nutr, 46 (5), 251-56. PubMed: 17497074
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Nava-Villalba, M and C Aceves (2014), ‘6-iodolactone, key mediator of antitumoral properties of iodine.’, Prostaglandins Other Lipid Mediat, 112 27-33. PubMed: 25018052
Patrick, L (2008), ‘Iodine: deficiency and therapeutic considerations.’, Altern Med Rev, 13 (2), 116-27. PubMed: 18590348
Rösner, H, et al. (2016), ‘Antiproliferative/cytotoxic effects of molecular iodine, povidone-iodine and Lugol’s solution in different human carcinoma cell lines.’, Oncol Lett, 12 (3), 2159-62. PubMed: 27602156
Shah, NM, et al. (1986), ‘Iodoprotein formation by rat mammary glands during pregnancy and early postpartum period.’, Proc Soc Exp Biol Med, 181 (3), 443-49. PubMed: 3945653
Smyth, PP, et al. (1996), ‘A direct relationship between thyroid enlargement and breast cancer.’, J Clin Endocrinol Metab, 81 (3), 937-41. PubMed: 8772554
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